ArticleDevelopment (Cambridge, England)2008
The Mn1 transcription factor acts upstream of Tbx22 and preferentially regulates posterior palate growth in mice.
Article in Development (Cambridge, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
45 citing papers in PubMed, 75 citations in OpenAlex.
- A Novel Nonsense Variant in TBX15 Transcription Factor Suggests an Expanded Genetic Spectrum Of Submucous Cleft Palate.International dental journal · 2026Article
- Evolution of the essential geneProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Molecular Regulation of Palatogenesis and Clefting: An Integrative Analysis of Genetic, Epigenetic Networks, and Environmental Interactions.International journal of molecular sciences · 2025Review
- Novel insights into palatal shelf elevation dynamics in normal mouse embryos.Frontiers in cell and developmental biology · 2025Article
- A cell type-aware framework for nominating non-coding variants in Mendelian regulatory disorders.Nature communications · 2024Article
- A cell type-aware framework for nominating non-coding variants in Mendelian regulatory disorders.medRxiv : the preprint server for health sciences · 2023Article
- A Novel Pathogenic Variant in theJournal of pediatric genetics · 2023Article
- Gene Regulatory Networks and Signaling Pathways in Palatogenesis and Cleft Palate: A Comprehensive Review.Cells · 2023Review
- Ranbp1 modulates morphogenesis of the craniofacial midline in mouse models of 22q11.2 deletion syndrome.Human molecular genetics · 2023Article
- Canonical Wnt signaling regulates soft palate development by mediating ciliary homeostasis.Development (Cambridge, England) · 2023Article
- Diagnosis and treatment of MN1 C-terminal truncation syndrome.Molecular genetics & genomic medicine · 2022Article
- Revisiting the embryogenesis of lip and palate development.Oral diseases · 2022Review
- Osteogenic and angiogenic profiles of the palatal process of the maxilla and the palatal process of the palatine bone.Journal of anatomy · 2022Article
- MN1 gene loss-of-function mutation causes cleft palate in a pedigree.Brain : a journal of neurology · 2021Article
- Article
- Alteration of DNA Damage Response Causes Cleft Palate.Frontiers in physiology · 2021Article
- Gain-of-Function MN1 Truncation Variants Cause a Recognizable Syndrome with Craniofacial and Brain Abnormalities.American journal of human genetics · 2020Article
- MN1 C-terminal truncation syndrome is a novel neurodevelopmental and craniofacial disorder with partial rhombencephalosynapsis.Brain : a journal of neurology · 2020Article
- Shox2 regulates osteogenic differentiation and pattern formation during hard palate development in mice.The Journal of biological chemistry · 2019Article
- Regulatory Mechanisms of Soft Palate Development and Malformations.Journal of dental research · 2019Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The mammalian secondary palate exhibits morphological, pathological and molecular heterogeneity along the anteroposterior axis. Although the cell proliferation rates are similar in the anterior and posterior regions during palatal outgrowth, previous studies have identified several signaling pathways and transcription factors that specifically regulate the growth of the anterior palate. By contrast, no factor has been shown to preferentially regulate posterior palatal growth. Here, we show that mice lacking the transcription factor Mn1 have defects in posterior but not anterior palatal growth. We show that Mn1 mRNA exhibits differential expression along the anteroposterior axis of the developing secondary palate, with preferential expression in the middle and posterior regions during palatal outgrowth. Extensive analyses of palatal gene expression in wild-type and Mn1(-/-) mutant mice identified Tbx22, the mouse homolog of the human X-linked cleft palate gene, as a putative downstream target of Mn1 transcriptional activation. Tbx22 exhibits a similar pattern of expression with that of Mn1 along the anteroposterior axis of the developing palatal shelves and its expression is specifically downregulated in Mn1(-/-) mutants. Moreover, we show that Mn1 activated reporter gene expression driven by either the human or mouse Tbx22 gene promoters in co-transfected NIH3T3 cells. Overexpression of Mn1 in NIH3T3 cells also increased endogenous Tbx22 mRNA expression in a dose-dependent manner. These data indicate that Mn1 and Tbx22 function in a novel molecular pathway regulating mammalian palate development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.